Venous Thromboembolism = DVT + PE
Best nursing interventions:
Early mobilization — ASAP post-op or post-injury
VTE prophylaxis within 72 hours (unless contraindicated)
e.g., Low molecular weight heparin (LMWH)
Sequential Compression Devices (SCDs)
Hydration
Monitor for calf pain, redness, or swelling
📌 SCI patients are at high risk due to immobility. VTE prophylaxis is a priority.
CPP = MAP - ICP
CPP → Pressure needed to ensure blood flow to the brain.
MAP (Mean Arterial Pressure) = (SBP+2×DBP)/3
ICP (Intracranial Pressure) = pressure inside skull
🧮 Example:
If MAP = 90 mmHg and ICP = 15 mmHg
→ CPP = 90 - 15 = 75 mmHg
✅ Normal CPP = 60–100 mmHg
< 50 mmHg → ischemia, neuronal death
< 30 mmHg → ischemia, incompatible with life
Goal: Reduce pressure, promote perfusion, and prevent herniation
Key Interventions:
HOB at 30° (not flat)
Maintain neutral head position
Prevent hypoxia/hypercapnia (e.g., adequate oxygenation)
Avoid suctioning unless necessary
Minimize stimuli (lights, noise, clustering care)
Administer:
Mannitol or Hypertonic Saline to reduce ICP
Hypertonic saline has a high concentration of sodium to draw water out of the brain tissue and into the blood vessels.
Antipyretics to prevent fever
Sedatives/analgesics to reduce agitation
Prevent seizures with anticonvulsants
⛔ Avoid lumbar puncture with high ICP → risk of herniation
✅ Normal ICP: 5–15 mmHg
Mildly elevated: 16–20 mmHg
Moderate: 21–30 mmHg
Severe: 31–40 mmHg
Critical: >40 mmHg
📌 Cushing’s Triad = late sign of high ICP = MEDICAL EMERGENCY!
Bradycardia
Hypertension with widened pulse pressure
Irregular respirations
ICP → Pressure within the skull occupied by the brain, blood, and CSF.
Monroe-Kellie doctrine state that the three components must remain at a constant volume; if one component increases, another must decrease to maintain ICP (skull cannot expand).
Brain herniation occurs from too much pressure (brain tissue shifts abnormally and compresses vital structures).
IVIG = Intravenous Immunoglobulin
Purpose:
Modulates/controls immune response to reduce severity of GBS.
Blocks harmful antibodies attacking nerves
Most effective within 2 weeks of symptom onset
Given over 5 days
📌 Used to speed recovery and reduce severity.
Autoimmune demyelinating condition (immune system mistakenly attacks the nerves).
Progression:
Ascending → weakness starts in lower extremities, moves upward
Symmetrical, rapidly progressive weakness
Max weakness in 4 weeks
Clinical Manifestations:
Weakness
Parathesis + pain
Hypotonia (AKA muscle floppiness)
Absent/depressed DTR
Muscle cramps/aches
Major risks:
Respiratory failure (watch for diaphragm paralysis)
Autonomic dysfunction (BP swings, dysrhythmias)
Immobility (muscle atrophy, VTE)
🧬 Often preceded by GI or respiratory infection
🦴 Compression of lumbosacral nerve roots (cauda equina)
Symptoms (red flags):
Asymmetric leg weakness
Flaccid paralysis of legs
Loss of sensation in "saddle" area (buttocks, inner thighs)
Bladder & bowel dysfunction (retention or incontinence)
Severe low back pain with radiculopathy
📌 MEDICAL EMERGENCY! Requires surgical decompression.
Autonomic Dysreflexia = Life-threatening emergency in SCI at T6 or above
Characterized by severely high BP and bradycardia from overreacting to stimuli.
✅ Causes (stimuli below T6):
Full bladder (most common)
Impaction
Tight clothing
Pressure ulcers, ingrown toenails
❌ Not a cause:
Hypoglycemia
Anxiety
Fever (not a direct cause)
📌 Look for sudden headache, HTN, bradycardia, sweating above injury, flushed face and upper chest above injury, and nasal congestion.